褪黑素对新生鼠胆红素脑损伤的保护机制研究

发布时间：2018-04-29 12:23

本文选题：褪黑素 + 胆红素脑病　；参考：《桂林医学院》2012年硕士论文

【摘要】：目的：探讨褪黑素(melatonin, MT)对新生鼠胆红素脑损伤的保护作用及其机制。方法：取SPF级5日龄SD大鼠90只,雌雄不限,完全随机分为3组：生理盐水对照组、胆红素脑病模型组、MT治疗组。MT治疗组在制作胆红素脑病动物模型基础上给予MT治疗,各组用免疫组化法检测脑海马组织BAX、BCL-2蛋白的表达变化,酶联免疫吸附法检测血清中神经元特异性烯醇化酶(NSE)的水平,水迷宫实验测试学习记忆能力。结果：MT治疗组海马神经细胞在各时间点,海马组织BAX阳性细胞率低于模型组(P0.05),高于对照组(P0.05);BCL-2阳性细胞各组均高于模型组(P0.05)高于对照组(P0.05);血清NSE水平均低于模型组(P0.05),高于对照组(P0.05);水迷宫实验：褪黑素治疗组在各时间点找到安全平台的潜伏期均明显短于模型组(P0.05),穿越平台次数较模型组明显增多,两组均低于对照组。结论：新生大鼠胆红素脑损伤后给予褪黑素干预,可以提高脑组织的bcl-2的表达,抑制bax的表达,降低NSE的表达,发挥神经保护作用,可以改善胆红素相关性脑损伤所致的学习记忆障碍。
[Abstract]:Aim: to investigate the protective effect of melatonin (MTL) on bilirubin brain injury in neonatal rats and its mechanism. Methods: ninety male and female SD rats of SPF grade 5 days old were randomly divided into 3 groups: saline control group, bilirubin encephalopathy model group, MT treatment group, and MT treatment group on the basis of making bilirubin encephalopathy animal model. The expression of BCL-2 protein in brain tissue was detected by immunohistochemistry, the level of neuron-specific enolase (NSE) in serum was detected by enzyme-linked immunosorbent assay (Elisa), and the ability of learning and memory was tested by water maze test. Results the hippocampal neurons in the treatment group were at different time points. The rate of BAX positive cells in hippocampal tissue was lower than that in the model group and higher than that in the control group (P 0.05). The serum NSE level was lower than that in the model group and higher than that in the control group (P 0.05). The water maze test showed that melatonin was treated with melatonin. The latency of finding safe platform at each time point in the group was significantly shorter than that in the model group (P 0.05), and the number of crossing the platform was significantly higher than that in the model group. Both groups were lower than the control group. Conclusion: administration of melatonin in neonatal rats with bilirubin brain injury can increase the expression of bcl-2, inhibit the expression of bax, decrease the expression of NSE, and play a neuroprotective role. It can improve the learning and memory impairment caused by bilirubin related brain injury.
【学位授予单位】：桂林医学院
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R722.17

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